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Rbm8a regulates neurogenesis and reduces Alzheimer's disease-associated pathology in the dentate gyrus of 5×FAD mice

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Neural Regeneration Research 2024年第4期19卷 863-871页

作者： Chenlu Zhu Xiao Ren Chen Liu Yawei Liu Yonggang Wang Department of Neurology Lanzhou University Second Hospital Department of Neurology The First Affiliated Hospital of Nanchang University Department of Neurology Xiaogan City Central Hospital Health Service Department of the Guard Bureau of the General Office of the Central Committee of the Communist Party of China Headache Center Department of NeurologyBeijing Tiantan HospitalCapital Medical University

Alzheimer’s disease is a prevalent and debilitating neurodegenerative condition that profoundly affects a patient’s daily functioning with progressive cognitive decline,which can be partly attributed to impaired hippocampal neurogenesis.Neurogenesis in the hippocampal dentate gyrus is likely to persist throughout life but declines with aging,especially in Alzheimer’s disease.Recent evidence indicated that RNA-binding protein 8A(Rbm8a)promotes the proliferation of neural progenitor cells,with lower expression levels observed in Alzheimer’s disease patients compared with healthy people.This study investigated the hypothesis that Rbm8a overexpression may enhance neurogenesis by promoting the proliferation of neural progenitor cells to improve memory impairment in Alzheimer’s disease.Therefore,Rbm8a overexpression was induced in the dentate gyrus of 5×FAD mice to validate this hypothesis.Elevated Rbm8a levels in the dentate gyrus triggered neurogenesis and abated pathological phenotypes(such as plaque formation,gliosis reaction,and dystrophic neurites),leading to ameliorated memory performance in 5×FAD mice.RNA sequencing data further substantiated these findings,showing the enrichment of differentially expressed genes involved in biological processes including neurogenesis,cell proliferation,and amyloid protein formation.In conclusion,overexpressing Rbm8a in the dentate gyrus of 5×FAD mouse brains improved cognitive function by ameliorating amyloid-beta-associated pathological phenotypes and enhancing neurogenesis.

关键词： adora2a Alzheimer’s disease astrocyte cAMP signaling pathway dentate gyrus dystrophic neurites microglia neurogenesis plaque Rbm8a

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Dietary adenosine supplementation improves placental angiogenesis in IUGR piglets by up-regulating adenosine A2a receptor

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Animal Nutrition 2023年第2期13卷 282-288页

作者： Zifang Wu Jiawei Nie Deyuan Wu Shuangbo Huang Jianzhao Chen Huajin Liang Xiangyu Hao Li Feng Hefeng Luo Chengquan Tan Guangdong Provincial Key Laboratory of Animal Nutrition Control National Engineering Research Center for Breeding Swine IndustryInstitute of Subtropical Animal Nutrition and FeedCollege of Animal ScienceSouth China Agricultural UniversityGuangzhouGuangdong 510642China Dekon Food and Agriculture Group ChengduChina

Abnormal placental angiogenesis is associated with the occurrence of intrauterine growth restriction(IUGR)in piglets,and effective treatment strategies against this occurrence remain to be explored.Adenosine has been reported to play an important role in angiogenesis,but its role in placental angio-genesis is still unknown.Here,we investigated the effect of dietary adenosine supplementation on IUGR occurrence in piglets by analyzing the role of adenosine in placental angiogenesis for Normal and IUGR piglets.Specifically,88 sows were allotted to 2 treatments(n=44)and fed a basal diet supplemented with 0%or 0.1%of adenosine from day 65 of gestation until farrowing,followed by collecting the placental samples of Normal and IUGR piglets,and recording their characteristics.The results showed that adenosine supplementation increased the mean birth weight of piglets(P2a receptor(adora2a)was lower(Padora2a expression,and also had an interaction effect between factors IUGR and Ado.Collectively,placentae for IUGR piglets showed impaired angiogenesis and down-regulated expression level of adora2a,while dietary adenosine supplementation could activate adora2a expression,improve the placental angio-genesis,and ultimately decrease the occurrence of IUGR in piglets.

关键词： Angiogenesis IUGR Placenta Adenosine adora2a

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adora2a基因多态性与中国汉族健康人群人格特质的相关性研究

ADORA2A基因多态性与中国汉族健康人群人格特质的相关性研究

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作者：刘璐中国医科大学

学位级别：硕士

目的:人格描述了在认知、情感、动机方面的精神状态的稳定的个体差异,而且这种精神状态导致了稳定的行为模式倾向。有三分之二的人格特质的差异是因为基因影响,因此人们进行基因多态性的相关研究试图找出影响人格特质的基因。5-HT及多... 详细信息

目的:人格描述了在认知、情感、动机方面的精神状态的稳定的个体差异,而且这种精神状态导致了稳定的行为模式倾向。有三分之二的人格特质的差异是因为基因影响,因此人们进行基因多态性的相关研究试图找出影响人格特质的基因。5-HT及多巴胺均与人格特质有关,且能对DA或5-HT产生影响的物质都可能与人格特质有关,并且这种联系可能与性别有关。adora2a活化可以影响多种受体,其对多巴胺受体有相关且抑制性作用,同时其本身也可影响学习记忆、习惯养成以及adora2a的缺乏会导致行为兴奋作用、攻击性增加及增强目的驱动性行为。并且adora2a被证实与多种神经系统疾病相关。因此我们猜测adora2a基因可能与人格特质相关,国内目前还没有相关研究,因此本研究采用聚合酶链式反应-限制性片段长度多态性（PCR-RFLP）方法检测adora2a基因多态性,探讨adora2a基因多态性与汉族健康人人格特质是否具有相关性。研究方法:本研究选取选取受试者共535人,其中男性259人,女性276人,排除精神疾病及重大躯体疾病病史。首先采用TPQ三维人格量表进行人格评定,当日采取外周静脉血2ml,碘化钾法提取DNA,采用PCR-RFLP测定基因型,用SPSS软件进行统计学分析,探究各基因型的健康人群组之间分数是否存在差异,P＜0.05被认为有显著统计学意义。结果:1.在汉族健康人群整体中,对于rs5996696位点,NS（X~2=1.366,P=0.505）、HA（X~2=1.143,P=0.565）、RD（X~2=2.310,P=0.315）在各基因型的分数均无明显差异;对于rs2298383位点,NS（X~2=3.101,P=0.212）、HA（X~2=4.161,P=0.125）、RD（X~2=0.748,P=0.688）在各基因型的分数均无明显差异,但HA4（X~2=6.134,P=0.047）在各基因型的分数存在明显差异。2.在性别分层中,对于rs5996696,在男性中NS（X~2=4.353,P=0.113）、HA（X~2=1.152,P=0.562）、RD（X~2=2.303,P=0.316）的分数在各基因型均无明显差异,但RD4（X~2=8.348,P=0.015）的分数在各基因型有显著性差异;在女性中NS（X~2=0.06,P=0.970）、HA（X~2=1.272,P=0.529）的分数在各基因型均无明显差异,但RD（X~2=6.135,P=0.047）的分数在各基因型有显著性差异。对于rs2298383,在男性中NS（X~2=2.417,P=0.299）、HA（X~2=0.971,P=0.615）、RD（X~2=4.907,P=0.086）的分数在各基因型均无明显差异,但NS3（X~2=7.793,P=0.020）的分数在各基因型有显著性差异;在女性中NS（X~2=2.473,P=0.290）、HA（X~2=4.604,P=0.100）、RD（X~2=0.463,P=0.793）的分数在各基因型均无明显差异,但HA4（X~2=6.210,P=0.045）的分数在各基因型有显著性差异。结论:研究表明adora2a基因多态性与汉族健康人群人格特质相关,adora2a基因可能是影响人格的一个潜在基因。

关键词： adora2a 基因多态性汉族健康人群人格特质

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Genetic Polymorphism of adora2a Is Associated With the Risk of Epilepsy and Predisposition to Neurologic Comorbidity in Chinese Southern Children

Genetic Polymorphism of ADORA2A Is Associated With the Risk ...

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2022第27届广东省药师周大会

作者： Xiaomei Fan Yuna Chen Wenzhou Li Hanbin Xia Bin Liu Huijuan Guo Yanxia Yang Chenshu Xu Shaojie Xie Xueqing Xu Department of Pharmacy Shenzhen Baoan Women's and Children's HospitalJinan University School of Pharmaceutical Sciences Health Science CenterShenzhen University

Epilepsy,a common disorder of the brain,exhibits a high morbidity rate in children.Childhood epilepsy(CE) is frequently comorbid with neurologic and developmental disorders,sharing under lyinggenetic factors.This study aimedto in vestigate the impact of adora2 A,BDNF,and NTRK2 genepoly morphismson the risk of childhood epilepsy and their associations with predisposition to epileptic comorbidities.A total of 444 children were enrolled in this study,and three single nucleotide polymorphisms,including adora2 A rs2298383,BDNF rs6265,and NTRK2 rs1778929,were genotyped.The frequency distribution of genotypes was compared not only between CE patients and healthy children but also between CE patients with and without comorbidities.The results indicated that the carriers of adora2 Ars2298383 TTgenotypetended to have alowerriskofepilepsy(OR=0.48,95%CI=0.30-0.76),while the CT genotype was related to ahigher risk(OR=1.56,95%CI=1.06-2.27).The ADO RA2 Ars2298383 CC genotypepre disposed CE patients to comorbid neurologic disorders(OR=2.76,95% CI=1.31-5.80).Genetic variations in BDNF rs6265 and NTRK2 rs1778929 had no significant association with CE and its comorbidities.Fourteen adora2 Atargetgenes related to epilepsy were identified by the protein-prote in interaction analysis,which were mainly involved in the biological processes of "negative regulation of neuron death" and "purine nucleoside biosynthetic process" through the gene function alenrichment analysis.Our study revealed that the genetic polymorphism of adora2 Ars2298383 was associated with CE risk and predisposition to neurologic comorbidity in children withepilepsy,and the involved mechanism mightberelated to the regulation of neuron death and purine nucleoside biosynthesis.

关键词： adora2a polymorphism childhood epilepsy neurologic comorbidity developmental comorbidity target-pathway analysis

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腺苷A2a受体基因多态性与北方汉族人群精神分裂症关联性研究

腺苷A2a受体基因多态性与北方汉族人群精神分裂症关联性研究

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作者：苗俊晓中国医科大学

学位级别：硕士

目的:精神分裂症是一种复杂的、严重的精神障碍,具有很强的遗传性,患者的主要表现为异常行为和认知综合征。精神分裂症的病因尚不明确,但与多种因素所导致的多巴胺源性失调和NMDA受体减弱密切相关。腺苷A2a受体在中枢神经中高度表达,参... 详细信息

目的:精神分裂症是一种复杂的、严重的精神障碍,具有很强的遗传性,患者的主要表现为异常行为和认知综合征。精神分裂症的病因尚不明确,但与多种因素所导致的多巴胺源性失调和NMDA受体减弱密切相关。腺苷A2a受体在中枢神经中高度表达,参与介导了神经元发育、睡眠与觉醒、学习与记忆、运动及药物成瘾等一系列重要过程,A2a受体的缺乏会导致异常的行为兴奋,攻击性增加。腺苷A2a受体与多巴胺D2受体共同分布于纹状体的腹侧和背侧,形成A2a/D2受体异源二聚体,两者作用相互抑制,在神经传递的调节和整合中起着关键作用。此外腺苷A2a受体还可以影响谷氨酸的释放和转运,大量的研究证据提示了腺苷A2a受体与精神分裂症病理机制的相关性。本实验选取了腺苷A2a受体蛋白基因的rs5996696和rs2298383两个位点分别进行单核苷酸多态性的研究,探讨腺苷A2a受体基因与中国北方汉族人群中精神分裂症的相关性。研究方法:本次研究共纳入精神分裂症组398人,健康对照组535人,采用聚合酶链式反应-限制性片段长度多态性（PCR-RFLP）方法检测腺苷A2a受体基因多态性,实验结果利用spss和haploview进行分析。结果:单核苷酸多态性与精神分裂症的关联分析:1.在病例组与对照组中,rs5996696位点基因型及等位基因分布在本次试验中并未发现统计学差异,rs2298383 T/C的C等位基因（X2=6.807;p=0.009;OR=1.278）和CC纯合子基因型（X2=7.826;p=0.005;OR=1.705）在两组有统计学差异。2.连锁不平衡检测中位点rs5996696和rs2298383（D′=0.943;r2=0.09）存在很强的连锁不平衡性,进一步单倍体分析发现单倍体型TA频率（X2=6.268;p=0.0123）和单体型CA频率（X2=7.012;p=0.0081）在病例组和对照组之间有统计学意义的显著差异。结论:1.腺苷A2a受体基因单核苷酸多态性与中国北方汉族人群精神分裂症的发病风险具有相关性。2.rs2298383 T/C的C等位基因和CC纯合型可能是精神分裂症的危险因素。3.rs2298383 T/C和rs5996696 A/C的单体型CA可能是精神分裂症发病的潜在危险因素。4.rs2298383 T/C和rs5996696 A/C的单体型TA可能为精神分裂症的潜在保护因子。

关键词： adora2a 精神分裂症基因多态性

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